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Molecular Human Reproduction, Vol. 5, No. 2, 96-103, February 1999
© 1999 European Society of Human Reproduction and Embryology

The mechanism of action of epidermal growth factor and transforming growth factor {alpha} on aromatase activity in granulosa cells from polycystic ovaries*

Aileen Misajon1, Paul Hutchinson2, Nicholas Lolatgis3, Alan O. Trounson1 and Ghanim Almahbobi1,4

1 Centre for Early Human Development, Institute of Reproduction and Development, 2 Centre for Inflammatory Diseases, Monash University, and 3 Monash IVF, Clayton, Victoria 3168, Australia

We investigated aromatization and the mechanism of action of epidermal growth factor (EGF) and transforming growth factor {alpha} (TGF{alpha}) on oestradiol biosynthesis in freshly prepared granulosa cells from polycystic ovaries. Freshly prepared granulosa cells from polycystic ovaries incubated for only 3 h under basal conditions secreted significantly (P < 0.001) greater amounts of oestradiol-17ß than that of granulosa cells from normal ovaries. 8-Bromo-cyclic adenosine monophosphate (8-Br-cAMP), but not follicle stimulating hormone (FSH) or luteinizing hormone (LH), further enhanced this activity. Both EGF and TGF{alpha} inhibited gonadotrophin- or 8-Br-cAMP-stimulated, but not basal, oestradiol production. LH receptor (LHR) binding, estimated by immunolabelling the bound LH, was significantly (P < 0.001) reduced in granulosa cells from polycystic ovaries when compared with cells from normal ovaries. EGF or TGF{alpha} significantly reduced the binding in cultured cells from all patient groups (P < 0.05). More interestingly, a further increase of the inhibitory effect was seen in granulosa cells from polycystic ovaries (P < 0.001). In conclusion, granulosa cells from polycystic ovaries contain high levels of basal aromatase activity in vitro, which is probably inherited from the in-vivo condition. EGF and TGF{alpha} suppress oestradiol synthesis at a step beyond the production of cAMP and also LHR binding with more effect in granulosa cells from polycystic ovaries.

aromatase/gonadotrophins/growth factors/PCOS

*This paper was presented at the 13th Annual Meeting of the European Society of Human Reproduction and Embryology (ESHRE), Edinburgh, UK, 1997.

4 To whom correspondence should be addressed at: Institute of Reproduction and Development, Block B, Level 5, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria, 3168, Australia


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